Plant-parasitic nematodes (PPNs), such as root-knot nematodes (RKNs) and cyst nematodes (CNs), are among the most devastating pests in agriculture. RKNs and CNs induce redifferentiation of root cells into feeding cells, which provide water and nutrients to these nematodes. Plants trigger immune responses to PPN infection by recognizing PPN invasion through several different but complementary systems. Plants recognize pathogen-associated molecular patterns (PAMPs) sderived from PPNs by cell surface–localized pattern recognition receptors (PRRs), leading to pattern-triggered immunity (PTI). Plants can also recognize tissue and cellular damage caused by invasion or migration of PPNs through PRR-based recognition of damage-associated molecular patterns (DAMPs). Resistant plants have the added ability to recognize PPN effectors via intracellular nucleotide-binding domain leucine-rich repeat (NLR)-type immune receptors, leading to NLR-triggered immunity. Some PRRs may also recognize apoplastic PPN effectors and induce PTI. Plant immune responses against PPNs include the secretion of anti-nematode enzymes, the production of anti-nematode compounds, cell wall reinforcement, production of reactive oxygen species and nitric oxide, and hypersensitive response–mediated cell death. In this review, we summarize the recognition mechanisms for PPN infection and what is known about PPN-induced immune responses in plants.

The retinal pigment epithelium (RPE) forms the outer blood-retinal barrier between neural retina and choroid. The RPE has several important vision supporting functions, such as transport mechanisms that may also modify pharmacokinetics in the posterior eye segment. Expression of plasma membrane transporters in the RPE cells has not been quantitated. The aim of this study was to characterize and compare transporter protein expression in the ARPE19 cell line and hfRPE (human fetal RPE) cells by using quantitative targeted absolute proteomics (QTAP). Among 41 studied transporters, 16 proteins were expressed in hfRPE and 13 in ARPE19 cells. MRP1, MRP5, GLUT1, 4F2hc, TAUT, CAT1, LAT1, and MATE1 proteins were detected in both cell lines within 4-fold differences. MPR7, OAT2 and RFC1 were detected in the hfRPE cells, but their expression levels were below the limit of quantification in ARPE19 cells. PCFT was detected in both studied cell lines, but the expression was over 4-fold higher in hfRPE cells. MCT1, MCT4, MRP4, and Na/K ATPase were upregulated in the ARPE19 cell line showing over 4-fold differences in the quantitative expression values. Expression levels of 25 transporters were below the limit of quantification in both cell models. In conclusion, we present the first systematic and quantitative study on transporter protein expression in the plasma membranes of ARPE19 and hfRPE cells. Overall, transporter expression in the ARPE19 and hfRPE cells correlated well and the absolute expression levels were similar, but not identical. The presented quantitative expression levels could be a useful basis for further studies on drug permeation in the outer blood-retinal barrier.

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It is important to understand the molecular mechanisms of barrier disruption in the central nervous system (CNS) of patients with multiple sclerosis (MS). The purpose of the present study was to clarify whether claudin-11 is involved in the disruption of two endothelial barriers (blood-brain barrier (BBB) and blood-spinal cord barrier (BSCB)) and two epithelial barriers (blood-arachnoid barrier (BAB) and blood-CSF barrier (BCSFB)) in the CNS in MS. Immunohistochemical analysis revealed that, in both normal human and mouse, claudin-11 is co-localized with claudin-5 in the brain and spinal cord capillaries. The absolute protein expression level of claudin-11 was nearly equal to that of claudin-5 in rat brain capillaries, but was 2.81-fold greater in human brain capillaries. The protein expressions of claudin-11 were significantly downregulated in the brain and spinal cord capillaries of an MS patient and experimental autoimmune encephalomyelitis (EAE) mice. Specific downregulation of claudin-11 with siRNA significantly increased the transfer of membrane-impermeable FITC-dextran across human brain capillary endothelial cell (hCMEC/D3) monolayer. As for the epithelial barrier, claudin-11 protein expression was not decreased in choroid plexus epithelial cells forming the BCSFB in EAE mice, whereas it was decreased in brain and spinal cord meninges that form the BAB. Specific downregulation of claudin-11 with siRNA in a rat choroid plexus epithelial cell (TR-CSFB) monolayer significantly increased the permeability of FITC-dextran. In conclusion, our present findings indicate that claudin-11 expression at the BBB, BSCB, and BAB, but not the BCSFB, is downregulated in multiple sclerosis, impairing the functional integrity of these barriers.

Marginal zone (MZ) B cells produce a first wave of antibodies for protection from blood-borne pathogens. However, the role of MZ B cells in inflammatory responses has not been elucidated. Here we show that MZ B cells produce pro-inflammatory cytokines, such as interleukin-6 (IL-6), and exacerbate systemic inflammatory responses to lipopolysaccharide (LPS). After intravenous injection of LPS or E. coli, mice deficient in MZ B cells or IL-6 only in MZ B cells have attenuated systemic inflammatory responses and prolonged survival compared with wild-type mice. LPS directly stimulates MZ B cells via Toll-like receptor 4 (TLR4) and MyD88 pathways for IL-6 production. Furthermore, TLR4 requires physical and functional association with Fcα/μR (CD351) for its oligomer formation, NF-κB signalling and IL-6 production from MZ B cells; this association is responsible for systemic inflammatory responses and endotoxic shock. These results reveal a pro-inflammatory role of MZ B cells in endotoxic shock.

Isolation of splenic macrophage subpopulations using an enzyme cocktail

The smokybrown cockroach Periplaneta fuliginosa has spread all over the world, and is now one of the most undesired invasive alien pests in Japan. Because cockroaches are generally infected by thelastomatid nematodes, they are being distributed around the world with their parasitic nematodes. Nothing is known about parasitic nematode species in P. fuliginosa differences, or similarity of the parasite's population structures between the different countries of the host cockroaches. Here we investigated the P. fuliginosa invasive to Japan and found that 100% of individuals were infected with one nematode species. According to the morphology and the sequence of the D2/D3 expansion segment of the 28S ribosomal RNA gene, we identified the parasite as Leidynema appendiculata. This nematode reproduced by haplodiploidy and its developmental timing under various conditions is quite divergent. Their population in the hindgut of P. fuliginosa was controlled with a few adult females and a male. This is the first report of the thelastomatid nematode isolated from the smokybrown cockroach, and is the basis for our future research examining the origin, distribution route and immigration history of the cockroach and the impact of L. appendiculata on native Japanese cockroach species.

Root-knot nematodes (Meloidogyne spp.) cause serious damage to many crops globally. We report the high-quality genome sequence of Meloidogyne arenaria genotype A2-O.